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Biomedical subjects

T Shimazu

Publications and source records attributed to T Shimazu.

At least 217 records · Page 12Linked to original sources
PubMed1981

Somatostatin, insulin, and glucagon secretion from isolated perfused pancreas of obese rats.

A comparison of the somatostatin with the insulin and glucagon secretions in hypothalamic obesity and genetic obesity was made using the isolated perfused pancreas of rats. In our perfusion experiment, the somatostatin response to 19 mM arginine in the presence of 4.4 mM glucose was significantly greater in both ventromedial hypothalamus (VMH)-lesioned and Zucker fa/fa rats than in their controls, as was the perfusate insulin. The perfusate arginine-stimulated glucagon secretion appeared no different in obese and control rats. Because hyperinsulinemia in vivo and hyperresponses to arginine of perfusate insulin and somatostatin were observed in both VMH-lesioned and Zucker fa/fa rats, whereas the perfusate glucagon secretion in the presence of 4.4 mM glucose was unchanged by obesity, the secretory behavior of some pancreatic hormones seems similar in VMH-lesioned and Zucker fa/fa rats in certain conditions. These results suggest that some abnormalities of pancreatic hormone secretion may be caused by a mechanism common to obesity, whether caused experimentally or genetically.

Animals↗
PubMed1981

Modulation by the hypothalamus of glucagon and insulin secretion in rabbits: studies with electrical and chemical stimulations.

The effects of electrical and chemical stimulations of the hypothalamus on the plasma levels of glucagon, insulin, and glucose were studied in undisturbed and free-moving rabbits. Electrical stimulation of the ventromedial hypothalamic nucleus (VMH) caused a marked increase in the circulating level of glucagon coincident with a rapid rise in the glucose level. The level of insulin did not increase during VMH stimulation, but increased after cessation of stimulation. Electrical stimulation of the lateral hypothalamic nucleus (LHN), on the other hand, did not alter the plasma level of either hormone. Microinjection of a minute amount of acetylcholine into the VMH led to a rapid increase in plasma glucagon, with a gradual rise in plasma glucose, but no significant change in the insulin level. The responses of glucagon and glucose to acetylcholine were almost completely blocked by previous treatment of the VMH with hexamethonium, but not with atropine. Microinjections of epinephrine and norepinephrine into the VMH also caused rises in the levels of both glucagon and insulin, although the effects of norepinephrine were much less than those of epinephrine. Injections of dopamine, serotonin, and gamma-aminobutyric acid had no effect. Chemical stimulation of the LHN only with epinephrine induced a preferential rise in the insulin level without any significant change in the levels of glucagon and glucose. It is concluded that the actions of acetylcholine in the VMH, probably though activation of nicotinic receptor, and of epinephrine in the LHN are important for hypothalamic modulation of the selective releases of glucagon and insulin, respectively. (Endocrinology 108: 605, 1981)

Acetylcholine↗
PubMed1981

Central nervous system regulation of liver and adipose tissue metabolism.

Hypothalamic and autonomic nervous regulation of carbohydrate and amino acid metabolism in the liver and of lipid metabolism in adipose tissues is described. The direct neural mechanism underlying this regulation has been evaluated. Electrical stimulation of the ventromedial hypothalamic nucleus (VMH)-splanchnic nerve system causes glycogenolysis in the liver by rapid activation of glycogen phosphorylase, whereas electrical stimulation of the lateral hypothalamic nucleus (LH)-vagus nerve system promotes glycogenesis in the liver by activation of glycogen synthetase, through direct neural and neural-hormonal mechanisms. Studies on chemical coding of the hypothalamic neurones have revealed that norepinephrine-sensitive neurones in the VMH and acetylcholine-sensitive neurones in the LH are specifically involved in the regulation of liver phosphorylase and glycogen synthetase, respectively. Acetylcholine-sensitive neurones of the LH were also found to be concerned in regulation of hepatic tyrosine and aminotransferase activity, through intermediation of the cholinergic system in the LH-vagal pathway. Finally, it has been shown that the VMH acts as a regulatory centre for lipolysis in adipose tissues by modulating activation of the sympathetic nervous system. In addition, stimulation of the VMH enhanced lipogenesis in brown adipose tissue preferentially, probably through a mechanism mediated by sympathetic innervation of this tissue. The latter finding suggests that both the breakdown and resynthesis of triglycerides in brown adipose tissue, but not in white adipose tissue, are accelerated by stimulation of the VMH.

Adipose Tissue↗
PubMed1981

[Clinical studies of cefoxitin for the treatment of chronic respiratory tract infections (author's transl)].

1. Serum and sputum concentrations of cefoxitin were measured at fixed intervals following a one hour drip infusion of 2 g to a total of three patients with chronic respiratory tract diseases. The peak levels in serum were found to be 142.1-273.6 microgram/ml at the end of the infusion and those in sputum were found to be 0.92-2.30 microgram/ml at 2 to 4 hours after initiation of the infusion. 2. Cefoxitin was administered to a total of five patients with chronic respiratory tract infections who had failed to respond to the previous treatments with conventional antibiotics. The results were that in one case the therapeutic effect was judged as excellent, in three cases as good, and in one case it was difficult to evaluate. In all cases, there was no significant abnormality indicative of side effects regarding clinical symptoms and laboratory tests of renal and hepatic functions. In a view of the findings stated above, it is considered that cefoxitin is a new antibiotic which can be used for the treatment of chronic respiratory tract infections.

Aged↗
PubMed1981

[Relationship between intrauterine pressure and maternal hemodynamics (author's transl)].

Placental and renal cortical blood flow were measured by thermocouple method in 70 cases of late pregnant rabbits, 17 late pregnant dogs and 2 late pregnant monkeys. Intrauterine resting tonus in 148 primigravid and 74 multigravid women tended to increase towards the onset of labor, with maternal mean blood pressure elevating in close relation to the intrauterine pressure. Especially in primigravid women there was a strong tendency and intrauterine resting tonus was higher value in primigravidas than that in multigravidas. The increasing of intrauterine pressure by uterine contraction caused an elevation of maternal blood pressure by about 10% in pregnant women, and caused a decrease of placental blood flow by about 30% respectively, but it did not show any definite pattern in renal cortical blood flow in experimental animals. On the other hand, the increasing of intrauterine resting tonus with intraamniotic saline injection in 47 cases of experimental animals brought about a decrease of placental blood flow by about 30%, at the same time caused a decrease of renal cortical blood flow by about 20% and an elevation of maternal blood pressure by about 10% respectively. These findings support the concept that increasing of uterine resting tonus could play a role in mediating late pregnancy induced hypertension.

Animals↗
PubMed1980

Regulation of liver phosphorylase phosphatase by glutathione disulfide.

The mechanism of inactivation of rabbit liver phosphorylase phosphatase by glutathione disulfide (GSSG) was investigated. The catalytic subunit of phosphorylase phosphatase was inactivated by GSSG and other disulfides. Inactivation by GSSG was a concentration-dependent process and resulted in the formation of an inactive, stable enzyme species. The inactivated enzyme could be reactivated by addition of various sulfhydryl compounds, including glutathione (GSH). Homogeneous phosphorylase phosphatase contains, per mol of catalytic subunit (Mr = 33,000), two sulfhydryl groups, one of which reacted with GSSG to form inactive enzyme. Binding studies with [glycine-2-3H]GSSG revealed simultaneous incorporation of 3H radioactivity into the catalytic subunit and stoichiometric loss of catalytic activity. Treatment of the 3H-labeled enzyme with GSH was accompanied by release of 3H radioactivity from the enzyme and restoration of enzyme activity. The results suggest that inactivation of phosphorylase phosphatase by GSSG results from the formation of a mixed disulfide between GSSG and one of the two sulfhydryl groups in the catalytic subunit.

Animals↗
PubMed1980

Circadian rhythm of liver glycogen metabolism in rats: effects of hypothalamic lesions.

The effects of electrolytic lesions of the suprachiasmatic nucleus (SCN) and ventromedial nucleus (VMH) of the hypothalamus on the circadian rhythm of liver glycogen metabolism were studied in rats fed during the dark period (2000-0800 h). Bilateral lesions of the SCN did not affect appreciably the circadian rhythmicity in three parameters of liver glycogen metabolism, i.e., glycogen content and glycogen synthetase I and phosphorylase a activities. In contrast, bilateral lesions of the VMH resulted in almost complete loss of circadian rhythmicity in phosphorylase a activity by lowering the high activity normally observed in late evening. VMH lesions also reduced the amplitudes of the rhythms of synthetase I activity and glycogen content, but did not abolish their rhythmicities. These results suggest that the integrity of the VMH, rather than the SCN, is important for regulation or expression of the food-triggered circadian rhythm of liver phosphorylase a activity. The implication of the lateral hypothalamic nucleus in regulation of the circadian rhythm of liver synthetase I is also discussed.

Animals↗
PubMed1978

Inactivation of phosphorylase phosphatase by a factor from rabbit liver and its chemical characterization as glutathione disulfide.

A factor inactivating phosphorylase phosphatase was isolated from rabbit liver. The isolation procedure consisted of heat treatment at 85 degrees C, extraction with n-butyl alcohol, and chromatography on Dowex 1 and DEAE-cellulose columns. The purified factor was different from the known protein inhibitors and was shown to be tripeptide composed of equimolar amounts of glutamic acid, cysteine, and glycine. The NH2-terminal and COOH-terminal amino acids were determined as glutamic acid and glycine, respectively. The factor was finally identified as glutathione disulfide by high voltage paper electrophoresis, paper chromatography, and liquid column chromatography using an amino acid analyzer. Addition of the purified factor or glutathione disulfide converted phosphorylase phosphatase to a stable, less active enzyme species, the extent of conversion depending on the amount added. The inactivated phosphatase was completely reactivated by addition of both glutathione (or 2-mercaptoethanol) and Mn2+ and partially reactivated by adding glutathione alone. Injection of glutathione disulfide into the portal vein of rabbits caused a rapid increase in phosphorylase alpha activity in the liver. These results suggest that glutathione disulfide is involved in regulation of phosphorylase activity in vivo, by causing inactivation of phosphorylase phosphatase in the liver.

Animals↗